SALT INTAKE AND SOFT DRINK CONSUMPTION IN CHILDREN
He FJ, Marrero NM, and MacGregor GA. Salt intake is related to soft drink consumption in children and adolescents. A link to obesity? Hypertension. 2008;51:629–634.
The link between salt intake and fluid intake is well characterized in adults. The World Health Organization has estimated that reducing daily salt intake by half, to ∼5 g/d, would reduce fluid intake by about 350 mL/d per person. While intake of water is seldom of concern, much of the fluids consumed in developed nations contribute significant calories to the daily diet. Soft drink intake in children, in particular, is a concern due to the proposed link between intake of sweetened beverages and obesity. To determine a link between salt intake and soft drink consumption, He et al. analyzed data from the National Diet and Nutrition Survey for young people in Great Britain. The survey, conducted in 1997, provides a representative sample of young people between the ages of 4 and 18 years.
Data from 1688 participants (837 girls) were included in the analysis of He et al. Average salt intake (excluding that used in cooking or at the table) was ∼4.6 g/d at age 4, and intake increased with age. By the age of 18, individuals were consuming ∼6.8 g/d. Mean fluid intakes varied with age, with younger children consuming less than older children (range ∼980–1300 mL/d). Approximately 30% of total fluid intake came from sugar-sweetened beverages. Salt intake was highly correlated with fluid intake, and regression analysis indicated that a 1 g/d reduction in salt intake would lead to a 100 g/d reduction in fluid intake. This study is the first to show a relationship between salt intake and fluid intake in children. Reduction of salt intake in general is a major public health goal, with the aim of reducing hypertension. The authors also posit that reduction of salt intake could potentially reduce obesity by limiting the amount of sweetened beverages children consume; however, this presumes that children will selectively reduce intake of sugar-sweetened beverages rather than reducing intake of beverages of all types.
Comment: Dr. Weinberger, in an accompanying editorial, addresses the conclusions drawn by He et al. Importantly, he notes that the relationship between sodium intake, caloric intake, and sweetened beverage consumption are not isolated variables in the recent rises in obesity in children and adolescents. Additionally, he observes that intake of sweetened beverages remains relatively constant, and he raises the point that salt intake may affect hedonic preference for sweetened beverages, but that this has not been adequately explored.
Editorial Comment: Weinberger MH. Are children doomed by what they eat and drink? Hypertension. 2008;51:615–616.
VITAMIN K AND HIP FRACTURE
Yaegashi Y, Onoda T, Tanno K, Kuribayashi T, Sakata K, and Orimo H. Association of hip fracture incidence and intake of calcium, magnesium, vitamin D, and vitamin K. Eur J Epidemiol. 2008;23:219–225.
Hip fracture is a common and serious outcome of osteoporosis, which can lead to loss of independence and decreased quality of life in the elderly. Nutrients such as calcium, magnesium, and vitamins D and K are recognized for their importance in bone metabolism. Vitamin K has only recently gained attention for its proposed role in bone health, perhaps through positive effects on calcium balance. Yaegashi et al. explored national intake patterns of calcium, magnesium, and vitamins D and K and related intake levels to incidence of hip fracture in Japanese men and women.
The estimated number of hip fractures in 2002 was 211,600 (93,100 women), with different rates seen in different regions of the country. Fracture incidence was inversely correlated with regional intakes of vitamin K. In eastern Japan, high intake of vitamin K was associated with low incidence of hip fracture. In western areas of Japan, low vitamin K intake was associated with high incidence of hip fracture. It should be noted that the comparisons made in this study did not correlate intakes in individuals with or without hip fracture, but were made between national survey data. More research is needed to clearly establish the relationship between vitamin K and risk for hip fracture. The authors suggest that reconsidering the dietary reference intake of vitamin K from the perspective of osteoporosis is warranted.
HOMOCYSTEINE LOWERING AND PLASMA PHOSPHATIDYLCHOLINE
Crowe FL, Skeaff CM, McMahon JA, Williams SM, and Green TJ. Lowering plasma homocysteine concentrations of older men and women with folate, vitamin B-12, and vitamin B-6 does not affect the proportion of (n-3) long chain polyunsaturated fatty acids in plasma phosphatidylcholine. J Nutr. 2008;138:551–555.
High levels of circulating homocysteine are associated with increased risk of cardiovascular disease (CVD). Although reasonable hypotheses have been made regarding the role of B vitamin deficiency in elevated homocysteine, and trials have examined the ability of homocysteine-lowering treatments to prevent CVD, these trials have not been overly successful at reducing CVD even in the presence of reduced homocysteine. It is likely, therefore, that these trials have been confounded by other, unmeasured risk factors. One proposed risk factor is plasma levels of n-3 long chain polyunsaturated fatty acids (n-3 PUFA). Some research shows that low folate status or high homocysteine can decrease the proportion of n-3 PUFA, and administration of folate can increase the proportion of n-3 PUFA. In humans, research on this relationship is limited, however. Crowe et al. report on data from a randomized controlled study examining the effect of folate, B6, and B12 on the fatty acid composition in plasma phosphatidylcholine in individuals 65 years of age or older.
Participants received either a capsule containing 1000 µg folate, 500 µg vitamin B12, and 10 mg vitamin B6 (n = 123), or placebo (n = 120) daily for 2 years. Fasting plasma samples were taken at baseline and at 6-month intervals. Plasma homocysteine was significantly reduced and plasma folate and B12 were significantly elevated following intake of the supplement in comparison to placebo. The proportions of fatty acids in phosphatidylcholine were not affected by B vitamin intake. These data suggest that homocysteine or B vitamin intake may not affect the metabolism of n-3 PUFA. Although intake of the B vitamin supplement successfully lowered plasma homocysteine, plasma fatty acid proportions were not affected, providing one avenue to explore in the complex relationship among nutrient status, homocysteine, and CVD.
ANTIOXIDANT INTAKE AND DEMENTIA RISK
Gray SL, Anderson ML, Crane PK, Breitner JC, McCormick W, Bowen JD, Teri L, Larson E. Antioxidant vitamin supplement use and risk of dementia or Alzheimer's disease in older adults. J Am Geriatr Soc. 2008;56:291–295.
The antioxidant vitamins C and E have long been thought to play an important role in offsetting oxidative stress and subsequent disease. Epidemiological studies demonstrate a link between diets rich in antioxidants and reduced risk for Alzheimer's disease or vascular dementia. However, trials using supplements of vitamin C or vitamin E have shown no benefit in Alzheimer's disease risk. Gray et al. describe a prospective cohort study designed to examine the use of vitamins C and E, alone or in combination, and subsequent incidence of dementia or Alzheimer's disease.
Participants from the Adult Changes in Thought study were followed for an average of 5.5 years to identify dementia and Alzheimer's disease (n = 2969). Supplement use was determined by self-report of intake for at least 1 week in the month prior to baseline. During follow-up, 405 participants were diagnosed with dementia. Intake of vitamins C and E, alone or in combination, was not associated with a reduction in risk for developing dementia. A weakness of this study is the imprecise measurement of duration, frequency, and dose of antioxidant intake, and the reliance on participant self-report. For example, it is possible that as people progress into dementia, reports of supplement intake would become increasingly unreliable. Although many researchers propose a link between oxidative stress and the etiology of Alzheimer's disease and vascular dementias, hard evidence for the role of antioxidant supplements in preventing cognitive decline and onset of neuropathology remains elusive.
UTILITY OF GLUCOSAMINE SULFATE IN OSTEOARTHRITIS
Rozendaal RM, Koes BW, van Osch GJ, Uitterlinden EJ, Garling EH, Willemsen SP, Ginai AZ, Verhaar JA, Weinans H, and Bierma-Zeinstra SM. Effect of glucosamine sulfate on hip osteoarthritis: a randomized trial. Ann Intern Med. 2008;148:268–277.
Although widely used to treat symptoms of osteoarthritis, the efficacy of glucosamine sulfate in mediating pain and functioning in arthritis sufferers has not been established. Furthermore, many studies examine the effect of glucosamine in knee osteoarthritis, but its efficacy in hip osteoarthritis has not been reported. Rozendaal et al. conducted a 2-year randomized controlled trial comparing the effects of 1500 mg glucosamine sulfate and placebo on the progression of hip osteoarthritis.
Primary outcome measures included pain and function scores and joint space narrowing. A total of 207 individuals completed the 2-year trial (placebo n = 103, ∼70% women; glucosamine n = 104, ∼68% women). The results indicated glucosamine was not different from placebo in modifying the progression of hip osteoarthritis as determined by joint space narrowing or pain and function scores. The authors suggest that some studies show a benefit of glucosamine in the management of less severe osteoarthritis symptoms relative to more severe symptoms, although the severity of osteoarthritis in the present population was similar to that in other studies showing a benefit.
Comment: Glucosamine sulfate is thought to have its primary effect on preventing the loss of cartilage in osteoarthritis. Drs. Bijlsma and Lafeber suggest that the progression of osteoarthritis in the Rozendaal et al. study may have been too slow to see positive effects of glucosamine sulfate. In the present study, they argue, the loss of cartilage did not proceed at a rate that could be realistically treated with glucosamine supplementation. They suggest that a similar trial in individuals with more advanced osteoarthritis, where cartilage loss occurs more rapidly, would allow differences between glucosamine and placebo to be seen.
Editorial Comment: Bijlsma JW and Lafeber FP. Glucosamine sulfate in osteoarthritis: the jury is still out. Ann Intern Med. 2008;148:315–316.